Marion, Mitchell S.

AbstractOuter hair cell (OHC) metabolism is blocked by cisplatin. Concurrent changes in the renal handling of magnesium occur because of the damage cisplatin causes to the renal proximal tubule cells within the thick ascending loop of Henle. Although there is no evidence of cisplatin within the OHCs, there are significant levels of intracellular calcium, the antagonist to magnesium at the cell membrane. The OHC motile response is dependent on intracellular calcium. When the calcium current is suppressed by an antagonist, the extracellular OHC microphonic potential decreases. Magnesium deficiency is known to produce hyperexcitabililty within the central nervous system, including fatal audiogenic seizures. In addition, increases in the amplitude of the auditory brainstem response wave V occur with aminoglycoside therapy and magnesium deficiency. This paper illustrates the amplitude growth of distortion product otoacoustic emissions in two patients treated with cisplatin and explores the possible underlying reasons why this may be related to magnesium metabolism. Abbreviations: DPOAEs = distortion product otoacoustic emissions, OAEs = otoacoustic emissions, OHC = outer hair cell, TEOAEs = transient otoacoustic emissions

Aseptic meningitis is a rare complication of nonsteroidal anti-inflammatory drug (NSAID) use. Otologic symptoms may include sensorineural hearing loss and tinnitus. A 66-year-old woman sought the care of an otologist for sudden bilateral sensorineural hearing loss and a substantial increase in baseline tinnitus. The patient had previously undergone a left tympanoplasty secondary to cholesteatoma and had been treated for atypical face pain with Ibuprofen taken every six hours for three months. Magnetic resonance imaging (MRI) with gadolinium demonstrated abnormal enhancement of the dura mater and the surrounding basal cisterns, with extension of enhancing dura mater into the internal auditory canals. Cerebrospinal fluid examination revealed evidence of aseptic meningitis. An audiogram confirmed new bilateral sensorineural hearing loss. Hearing loss and tinnitus resolved and no abnormalities were observed with MRI when nonsteroidal anti-inflammatory medication was discontinued. Otolaryngologists are well aware of the otologic sequelae in patients with meningitis. However, NSAIDs need to be considered as possible causal agents in the evaluation of meningitis with otologic symptoms.

Labyrinthitis ossificans may be a hindrance to cochlear implantation by making electrode insertion difficult. We performed a histopathologic study of 24 temporal bones with labyrinthitis ossificans from multiple causes. The organ of Corti was graphically reconstructed and the degree of obstruction was estimated for each millimeter of the cochlea. Correlations were calculated between the degree of new bone formation and the cause, patient's age and sex, and time from the original temporal bone insult. Our results demonstrate that complete cochlear ossification is rare. The scala tympani in the basal turn of the cochlea is the most frequent area of ossification, regardless of the cause of the labyrinthitis ossificans. Meningogenic labyrinthitis, usually a childhood disease, was associated with the greatest amount of ossification. When ossification resulted from tympanogenic labyrinthitis, the scala tympani was completely ossified near the round window niche in all temporal bones. Neo‐ossification of the basal turn associated with otosclerosis was limited to the proximal 6 mm of the scala tympani in all cases. Three temporal bones had a patent round window niche and basal turn, but significant apical and middle‐turn ossification. Peripheral sensorineural elements were severely degenerated in the region of the ossification in all specimens, and spiral ganglion cell counts were decreased.

Injection of autologous adipose tissue removed via liposuction has been used clinically for facial contouring, the aging face, furrows, facial atrophy, acne scars, nasolabial folds, chin, and various other surgical defects. Survival rates for autografts of fat have been quoted anywhere from 30% to 80%. Our study uses a reproducible rabbit animal model for autotransplantation of adipose tissue and examines the histopathologic changes that occur to the graft over time. Autogenous subcutaneous fat was removed from a dorsal scapular donor site, treated to stimulate cannula damage as in liposuction, then reinjected at the base of the ear. Histologic examination of the grafts were made at 5, 10, 15, 20, 40, and 100 days after transplantation. Hematoxylin‐eosin sections were graded on degree of fibrosis present (0 to 4+), viable fat (1 to 10), degree of inflammation (0 to 4+), and neovascularization (+ or ‐). Viability of fat decreased from 8.5 to 10 at 5 days to 2 viability at 40 days. Acute inflammation peaked at 10 days, followed by the chronic inflammatory response with macrophages and multinucleated giant cells scavenging the dying fat graft. Neovascularization began at 5 days, peaked at 10 days, and remained constant thereafter only at the edge of the graft. Microcysts appeared at 15 days and increased in number in proportion to the decrease in viable fat. In summary, the temporal histologic events are progressive fibrosis; decreased amount of viable fat; inflammation beginning with a neutrophilic response, later a macrophage and giant cell response; and neovascularization at the periphery of the graft insufficient to maintain graft viability. In our animal model, autografts of fat appear to have limited long‐term viability and are replaced by fibrous tissue. This may have clinical implications in autografting of fat in facial plastic and reconstructive surgery.